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Pharmacology > !Neuropharmacology Clin Med > Flashcards

!Neuropharmacology Clin Med Flashcards

1
Q

What is a primary head ache

A

Benign disorder

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2
Q

What is a secondary headache

A

Sign of organic disease

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3
Q

What are the types of primary headaches

A

Migraine(with or without aura)

  • chronic migraine
  • tension type
  • cluster
  • post traumatic
  • drug rebound
  • trigeminal neuralgia
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4
Q

Headache history

A

How many types
Frequency

Pain

Prodrome (changes in energy levels, mood appetite, fatigue, muscle aches aura)

Associated symptoms-nausea, vomiting, anorexia, photophobia, photophobia, diarrhea, dizzy, behavior (retreat to dark, paces, rocks)

Previous medications tried

Medical/surgical history
Family history

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5
Q

Head ache exam

A

General examination (vitals, cardiac, extracranial, ROM C spine)

Neuro exam

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6
Q

Worrisome signs with headache

A

Worst HA

Onset after 50

Atypical for patent

Abrupt onset
Subacute with progressive worsening

Drowsi, confusion, memory

Weakness, ataxia, loss of coordination

  • paresthesia/sensory loss/analysis
  • abnormal medical or neuro exam
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7
Q

Diagnostic evaluation HA

A

Lab test, neurodiagnostic tests

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8
Q

What labs run with HA

A

CT, MRI/MRA, EEG, L.P. Arteriogram

-dental ENT allergy

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9
Q

As a general rule, HA patient should have a one-time, thurought neuro study

A

CT head with and without MRI of head

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10
Q

What do if have worrisome history or abnormal exam

A

Urgent imaging study and perhaps even and LP and arteriogram

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11
Q

CT can miss _% of subarachnoid hemorrhages and an LP may be needed if CT is normal

A

5-10%

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12
Q

What is difference between common and classic migraine

A

Common-no aura

Classic-aura

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13
Q

Intensity of common migraine

A

Moderate to severe

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14
Q

Disability common migraine

A

Inhibits or prohibits daily activities, pain aggravated by activity

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15
Q

Age onset common migraine

A

Late teens to early 20s

Prevalence peaks 35-40

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16
Q

Female:male ration for common migraine

A

3:1

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17
Q

Frequency common migraine

A

1-4 attacks per month (occasional) but 14 days or fewer per month

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18
Q

Duration common migraine

A

4 to 72 hours

Usually 12-24

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19
Q

Location common migraine

A

Unilateral or bilateral

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20
Q

Description common migraine

A

Throbbing/sharp/pressure

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21
Q

Prodrome common migraine

A

Mood changes, myalgia, food cravings, sluggishness, excessive yawning

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22
Q

Post drone common migraine

A

Fatigue, irritability, fog

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23
Q

Behavior common migraine

A

Retreat to dark, quiet room

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24
Q

Aura common migraine

A

None

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25
Q

_% of migraine sufferers don’t get aura

A

80-90

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26
Q

Associated symptoms of common migraine

A

Nausea, vomiting, photophobia, photophobia

Uncommon-diarrhea, conjunctival injection, stuffy nose, lacrimation, miosis, ptosis

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27
Q

Classic migraine

A

Aura (flashing lights or zig zag lines preceded migraine headache)

Aura lasts 15-30 minutes (scintillation, scotoma-often hemianopic)-but can be anything neurological

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28
Q

Chronic migrain

A

15 or more days per month, headache lasting 4 hours or longer, for a period of at least 3 months, not attributable to another disease

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29
Q

What causes migraines

A

Neurogenic inflammation
-trigeminal nerve becomes activated , releasing neuropeptides, causing painful neurogenic inflammation within the meninges, with subsequent effect on the dural vasculature (vasodilation, plasma protein extravasation, and mast cell degranulation)

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30
Q

Tension headache intensity

A

Mild to moderate

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31
Q

Tension HA disability

A

May inhibit but does not prohibit daily activities

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32
Q

Tension HA age of onset

A

Generally pear 20-40 years

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33
Q

Female to ace ration tension HA

A

3:2

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34
Q

Frequency tension HA episodic type

A

<15 days a month

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35
Q

Frequency tension HA chronic type

A

> 15 days a month?/ analgesic rebound HA, consider chronic migraine if intermittent migraines also present

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36
Q

Duration tension HA episodic

A

Several hours

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37
Q

Duration tensionHA chronic

A

All day, waxing and waning

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38
Q

Location tension HA

A

Bifrontal, bioccipital, neck, shoulders, band like

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39
Q

Description tension HA

A

Dull, aching, squeezing, pressure

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40
Q

Aura with tension HA

A

No

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41
Q

Behavior and tension HA

A

Not affected

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42
Q

Cluster HA intensity

A

Severe excruciating

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43
Q

Disability cluster HA

A

Prohibits daily activities

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44
Q

Age onset cluster HA

A

20s-50s

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45
Q

Female to male ration cluster HA

A

1:6

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46
Q

Cluster headache has recent association with __ _ _-

A

Obstructive sleep apnea

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47
Q

Cluster HA frequency episodic

A

1 or more a day for 6-8 weeks

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48
Q

Cluste HA frequency chronic

A

Several attacks per week without remission

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49
Q

Duration cluster HA

A

30 min-2 hr

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50
Q

Location cluster HA

A

100% unilateral, generally orbitotemporal

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51
Q

Pain of cluster HA

A

Non throbbing, excruciating sharp, boring, penetrating

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52
Q

Prodrome cluster ha

A

May include brief mild burning in ipsilateral inner canthus or internal nares

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53
Q

Aura cluster ha

A

No aura

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54
Q

Behavior cluster HA

A

Frenetic, pacing, rocking

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55
Q

Associated symptoms cluster HA

A

Ipsilateral ptosis, miosis, conjunctival injection, lacrimation, stuffed or runny nose

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56
Q

What triggers HA

A

Hormones, diet, stress, sensory stimuli

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57
Q

Hormones that trigger HA

A

Menses, ovulation, HRT, OC

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58
Q

Diet hat triggers HA

A

Alcohol , chocolate, aged cheese, MSG, aspartame, caffeine, nuts, nitrates/nitrites, citrus fruits, other

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59
Q

Changes that trigger migraine

A

Weather, seasons, travel, altitude, schedule, sleep patter, diet, skipping meals

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60
Q

Stress for HA trigger

A

Let down periods, intense activity, major life change/stress

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61
Q

Sensory stimuli of HA triggers

A

Bright or flickering lights odors

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62
Q

Acute treatment of migraine

A

OTC analgesics
NSAIDS-naproxen, ketorolac, diclofenac, isometheptene (midbrin), butalbital (fiorinal, fioricet)
Opoids-Demerol, morphine, codeine, oxycodone, hydrocodone
DHE nasal spray

Tristan’s

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63
Q

What are Triptans

A

5HT1 agonist

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64
Q

Name the triptans

A 
Sumatriptan
Zolmitriptan
Naratriptan
Rizatriptan
Almotriptan
Frovitriptan
Sumatriptan
Sumatriptan/long acting naproxen (treximet)
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65
Q

Triptans contraindicated in

A

Documented or strong risk factors for ischemic heart disease, other cardiovascular, cerebrovasculat or peripheral vascular disease, Raynaud syndrome, uncontrolled HTN, hemiplegic r basilar migraine, severe renal or hepatic impairment, use within 34 hours of tax with ergotamines, MAOIS or other 5HT1 agonists

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66
Q

Naratriptan dose

A

3.5 mg-one tablet at onset, may repeat 1 in 3 hr (max 10 mg in 24 hours)

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67
Q

Onset of action naratriptan

A

60 min

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68
Q

Benefits of naratriptan

A

Longest half life and fewest side effects

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69
Q

Contraindication for naratriptan

A

Patients with severe hepatic or renal impairment

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70
Q

Zolmitriptan dose

A

2.5,5 mg one at tablet onset HA may repeat 1 in 2 hours

Max 10 mg 24 hours

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71
Q

Onset action zolmitriptan

A

30-60 min

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72
Q

__ dose of solmitriptan recommended in patients with ___ impairment

A

Low hepatic

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73
Q

Sumatriptan dose

A

Up to 100 mg as a single dose and may repeat in 2 hours

Max 200 mg in 24

Onset 30-60min

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74
Q

Nasal spray sumatriptan

A

One spray at onset repeat 2 hours

Max 12 mg in 24 hours

Onset 10 min

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75
Q

Sumatriptan injection

A

One SQ at onset of MA, may repeat in 1 hr
Max 12 mg in 24 hours

Onset 10 min

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76
Q

Rizatriptan dose

A

One 5 or 10 mg tab at onset repeat in 24 hours
Max dose 20 mg in 24 hours

(Use 5 mg in patients on propranolol for max does of 10 in 24)

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77
Q

Almotriptan dose

A

12.5 mg tablets one at onset repeat 24 hours

Max 25 mg in 24 hours

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78
Q

Frovatriptan

A

2.5 tablet at onset repeat 1x in 24 hours

Max 7.5 in 24 hours

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79
Q

Frovatriptan

A
  1. 5 onset repeat two hours

7. 5 mg in 34 hours

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80
Q

If triptans doesn’t work

A

Try another , consider nasal or injectable if needed

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81
Q

What is the DHA protocol

A

Metoclopromide or prochlopereazine 10 mg IV over 60 sec. wait 5 min to allow distribution

Give DHE .5 mg IV over 60 sec wait 3-5 min
May repeat .5 mg IV if no relief every 8 hours for short term use

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82
Q

Contraindications DHE

A

Same as triptans

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83
Q

Side effects HE

A

Chest pressure, anxiety, speeding or dissociation of thoughts, nausea

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84
Q

If nausea/vomiting are a major feature of migraine, consider using a ____

A

Antimemtic like metoclopramide, prochloperazine

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85
Q

If insomnia is a major feature of migraine, consider a ____ or ___ to help patient sleep off migraine

A

Sedative-diazepam, temazepam

Tranquilizer-thorazine

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86
Q

A __ __ can sometimes be used to break the cycle of a prolonged migraine or several weeks of frequent migraines

A

Prednisone taper

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87
Q

What should you do if patient has one or more migraines a week

A

Preventative

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88
Q

Antidepressants to prevent migraines

A

TCA (amitriptyline, nortriptyline)
SSRI (fluoxetine, sertaline, escitalopram)
MAOI (phenelzine)
Beta blockers (propranolol)
Calcium channel blockers (verapamil)
Anticonvulsants (topiramate, valproic acid, gabapentin)
Ergot alkaloids (ergotomine+phenobarbital)
NSAIDS (ASA, naproxen)
Muscle relaxants (tizanidine)
Methysergide (sansert)

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89
Q

Botox injection

A

For chronic migraine

155 units into 31 sisters repeated 3 months

Need multiple treatments over 9-12 months to work

minimal side effects

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90
Q

Non prescription treatment of migraine

A

Exercise, stop smoking, HA education, riboflavin, mg, biofeedback/relaxation/stress management

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91
Q

What is one of the best preventative treatments of migraine and tension type HA

A

Stress management/relaxation/biofeedback

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92
Q

Acute treat of tension headache

A

OTC analgesics
NSAIDS
Opoids
Midbrain

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93
Q

Acute treat of tension HA

A

OTC analgesics
NSAIDs
Opoids
Midrin

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94
Q

Preventative treat for tension HA

A 
Antidepressents
-Tca, SSRI, MAOI
Muscle relaxant
Anticonvulsants
BOTOX injection 
Ergot alkaloids(DHE sometimes used to break cycle of chronic HA
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95
Q

Acute tc of cluster headache

A

DHE 1 mg IM or ergotamine 3 mg SL

Lidocaine 4% intranasal
Narcotics
Oxygen 6Lmin by mask
Sumatriptan 6 mg

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96
Q

Preventative treat for cluster headache

A 
Calcium channel blocker
Anticonvulsant
Lithium
Indomethacin
Prednisone 10-14 days
Ergotamine tartare
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97
Q

Trigeminal neuralgia

A

Excruciating sharp shooting electrical quality pain occurring in paroxysms in one or more distributions of the trigeminal nerve often frequent throughout the day.

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98
Q

Treat trigeminal neuralgia

A

Carbamazepine or oxcarbamazepine

Other anticonvulsants or surgery

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99
Q

Trigeminal autonomic cephalgias TAC

A

Group of headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomic features

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100
Q

What does TAC include

A 
Cluster HA
Paroxysmal hemicrania
Hemicrania continua
SUNCT syndrome 
SUNA syndrome
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101
Q

SUNCT syndrome

A

Short lasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing

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102
Q

Symptoms SUNCT

A

Excruciating, burning, stabbing electrical HA in periorbital area lasting seconds to a few minutes, occurring frequently throughout the day

Onset over 50 in men

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103
Q

Treat SUNCT

A

Anticonvulsants

LAMOTRIGINE

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104
Q

Paroxysmal hemicrania

A

Very similar to cluster headache (unilateral, periorbital, severe, excruciating, often with lacrimation, conjunctival irritation) but shorter duration (few minutes) and increased frequency (over 5 a day)

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105
Q

Treat paroxysmal hemicrania

A

Indomethacin

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106
Q

MS

A

Disorder of the brain and spinal cord characterized by a tendency for periods of increasing and decreasing symptoms and signs (exacerbation and remissions), which result from loss of nerve tract insulation (myelin) at multiple sites in the CNS

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107
Q

Common presentation of MS

A 
Paresthesias
Gait (transverse myelitis)
Weakness
Visual loss (optic neuritis)
Urinary difficulty
Dysarthria
Hemiparesis
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108
Q

Four types of MS

A 
Relapsing remitting (45-50%)
Secondary progressive (20-25%)
Primary progressive (15-20%)
Benign (20-15%
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109
Q

What is secondary progressive MS

A

Begin their disease process in the relapsing remitting category-includes some patients that still have occasional relapses (relapsing progressive

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110
Q

When is MS diagnosed

A

20s-30s

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111
Q

Characterization MS

A

Exacerbation and remission

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112
Q

Diagnose MS

A

No single test, multiple studies can help

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113
Q

Cause of MS

A

Unknown

Genetic, immune to CNS myelin triggers(virus and stuff)

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114
Q

Women or men MS

A

Women, but women more favorable course

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115
Q

With MS early onset is a more __ prognosis

A

Favorable

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116
Q

Tropical or temporal zones MS

A

Temperate

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117
Q

How diagnose MS

A

MRI of head, and C T spine
-ovoid lesions on T2W1 in periventricular white matter and in spinal cord
Multimodality evoked potentials (SSEPs, VEP, BAER

  • LP
  • oligoclonal bands and/or increased IgG index/synthesis rate are the typical findings in MS
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118
Q

Drugs for MS maintence

A 
Avonex, rebif
Betaseron
Cop a one
Tysabri
Gilenya
Tecfidera
Lemtrada
Zinbryta
Ocrevus
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119
Q

What is used t treat primary progressive MS in addition to relapsing forms of the disease

A

Ocrevus

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120
Q

How treat acute exacerbation in MS

A

High dose corticosteroids (methylprednisone-1 gram IV daily for 305 days followed by oral prednisone taper)-this reduces length of exacerbation but is not thought to change the voverall outcome of it

ACTH IVIg can be used on occasion, particularly in patients who do not tolerate traditional steroid treatment

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121
Q

CLinically Isolated SYndrome

A

A disease course of MS that can be monofocal or multifocal

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122
Q

Monofocal episode of clinically isolated syndrome

A

Person experiences a single neurologic sign or symptom that’s caused by a single lesion (optic neuritis in one eye)

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123
Q

Multifocal episode of clinically isolated syndrome/acute disseminated encephalomyelitis

A

More than one sign or symptom caused by lesions in more than one place (optic neuritis in one eye plus hemiparesis)

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124
Q

When do CIS patients have a high risk of developing MS

A

Multiple demyelinating lesions on MRI,

60-80% chance of developing in several years

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125
Q

When do CIS patients have a low risk of developing MS

A

Do not have multiple demyelinating lesions on MRI, have about a 20% chance of developing MS within several years

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126
Q

What disease may mimic MS

A 
Autoimmune disease-SLE with cerebritis or CNS vasculitis or polyarteritis nodosa with transverse myelitis
-Devics disease (neuromyelitis optica)
-b12 defiency
-lymphoma or leukemia within CNS
-spinocerebellum ataxia
-vascular malformations 
Infections
Granulomatous disease-sarcoidosis
-metachromatic leukodystrophy, adrenomyeloleukodystrophy
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127
Q

How manage spasticity of MS

A

Baclofen, tizanidine, diazepam, carbamazepine, Botox, dantrolene

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128
Q

How manage intention tremor

A

Propranolol, primidone, clonazepam

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129
Q

How manage urinary urgency

A

Oxybutinin

Destroy LA

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130
Q

How manage urinary retention/hesitancy

A

Bethanechol

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131
Q

Howmanage painful dysesthesias

A 
Carbamazepine
Oxcarbazepine
Gabapentin
Phenytoin
Baclofen
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132
Q

How manage fatigue

A

Amantadine, modafinil, armodafinil, buproprion, methylphenidate, pemoline, exercise

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133
Q

Cure for MS

A

No

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134
Q

Devics disease/neuromyelitis optica

A

Variant of MS, but probably a different entity

Inflammation, demyelination of optic nerves and spinal cord
Spare brain
Yeast for aquaporin 4 antibodies
-

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135
Q

How treat devics

A

Steroids, plasma exchange, followed by immunosuppression (azothiaprine, mycophenolate, mofetil, rituxumab)

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136
Q

What is paroxysmal disorders

A

Episodic!

-migraines, syncope, dizziness, seizure, transient global amnesia

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137
Q

Epilepsy

A

2 or more unprovoked seizures
4th most common neurological disorder
1/26 ppl will develop

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138
Q

Prejudice of epilepsy

A

Possessed by demons
Contagious
Up until 1965 illegal for epilepsy patients to marry in 17 states

Last state abolish in 1980

Can deny them in restaurants, theaters, and other public places until 1970s

Underemployment
Stopped in 1990 with American Disability act

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139
Q

% positive findings for epilepsy on a single EEG

A 
All types 40%
Generalized tonic closure 20%
Petit mal (with HV) 90%
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140
Q

Percent positive for epilepsy (al types) with 3 sleep-deprived EEG is __

A

85%

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141
Q

A normal EEG does not exclude the presence of ___

A

Epilepsy

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142
Q

Minor abnormalities on an EEG do not necessarily indicate a patient will have __

A

Seizures

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143
Q

Partial seizure (on one side of brain)

A

Simple partial
Complex partial
Secondarily generalized (partial onset)

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144
Q

Generalized seizures

A 
Absence (petit mal)
Tonic clinic
Myoclonic
Tonic
Clinic
Atonic
Clinic tonic clonic
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145
Q

Dimple partial seizure

A

Focal motor or sensory activity, no LOC, lasts seconds, no post octal state

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146
Q

Complex partial seizures

A

Non responsive staring, possible preceding aura, automatism, LOC, lasts 102 min, post-vital state

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147
Q

Characteristics of secondary generalized seizures

A

Bilateral tonic clonic activity, LOC, lasts 1-3 min, post entail state

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148
Q

Absence generalized seizures

A

Non responsive staring, rapid blinking, chewing, clonic hand motions, LOC, lasts 10-30 sec, no post octal state

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149
Q

Generalized tonic clonic seizures

A

Bilateral extension followed by symmetrical jerkingof extremities, LOC, lasts 1-3 min, post-ictal state

150
Q

Generalized atonic seizures

A

Sudden loss of muscle tone, head drops, or patient collapses, LOC, variable duration, post ictal state

151
Q

Myoclonic generalized seizures

A

Brief, rapid symmetrical jerking of extremities and/or torso, LOC, lasts < few seconds, minimal post ictal state

152
Q

What can we use to treat partialsecondary generalized seizures

A 
Valproic acid
Lamotrigine
Leciteracetam
Zonisamide
Perampanel
153
Q

What can we use to treat primary generalized seizures

A 
Valproic acid
Lemotrigine
Leviteracetam
Zonisamide
Perampanel
Topiramate
154
Q

One single combination of AEDs that has been shown to be synergistic in the treatment of epilepsy (espicially for primary generalized seizures) is __ ___ and ____

A

Valproic acid and lamotrigine

155
Q

Status epilepticus

A

Condition characterized by prolonged seizure (generally greater than 10 minutes or repeated seizures without recovery in between

156
Q

Treatment status epilepticus

A

ABC, IV
History
Labs:accuchek, CBC, chemistry panel, drug levels
Non-contrast CT head
Give benzodiazepine (lorazepam 2-4 mg IV)
-this buys time, but must give longer lasting AAED

-fosphenytoin (18mg/kg) IV (can give IM if no IV access possible) 100mg.min slow rate if BP drops

Phenobarbital-must incubate first, in anticipation for respiratoy depression

Valproic acid 500 mg every 4 hours-total 2000 mg in 24 hours

-lacks amide 200 mg every 12 hours (watch for cardiac conduction abnormalities)

If unsuccessful, try midazolam or propofol continuous IV drop (incubate)

Last resort: pentobarbital coma

In some cases a patient may only respond to one of the oral anticonvulsants (carbamazepine) consider establishing a nasogenic tube for administration

157
Q

General principles in treatment of epilepsy

A

Try monotherapy

Consider drug interactions -oral contraceptives with carbamazepine

Consider long term side effects-bone loss with carbamazepine of phenytoin

158
Q

All women of child bearing age should be on __ with 1 mg folic acid. This is important for women with epilepsy as many of the AEDs are folate depleting

159
Q

Pregnant women should avoid __ __

A

Valproic avid

160
Q

The newer antiepileptic drugs are safer in pregnancy than older ones but the drug of choice for a woman with epilepsy is the drug which best controls her seizures. What are new and old

A

New-lamotrigine, leviteracetam

Old—phenytoin or valproic acid

161
Q

Syncope

A

Pallor, sweating, abnormal head sensation, light head, positionally related, slow onset, brief unconsciousness

162
Q

Seizure

A

Urinary or bowel incontenance, tongue injury, tonic/clonic movements, postictal state

163
Q

Transient global ischemia

A

Sudden temporary isolated episode of loss of memory (amnesia)

No other neurologic symptoms or signs

Patient knows self and close family/friends, but may not recognize others

Usually lasts a few hours, then resolves

Usually doesn’t recur

164
Q

What are the two types of movement disorders

A

Bradykinetic

Hyperkinetic

165
Q

Bradykinetic disorders (a kinetic rigid syndromes)

A

Most common in Parkinsonism which encompasses many disorders:

  • idiopathic Parkinson’s disease
  • postencephalitic (Von Economos encephalitis
  • toxin induced (manganese, carbon disulfide, CO)
  • drug induced (metocolopramide, neuroepileptics like haloperidol, prochloperazine)
  • MPTP(meperidine analogue)
166
Q

Idiopathic parkinsons Disease cause

A

-depletion of dopamine int he nigrostriatal system , disrupting the balance of dopamine and acetylcholine

167
Q

Calincial findings idiopathic Parkinson’s disease

A

Tremor-resting tremor often unilateral at first pill rolling quality may see mouth or chin tremor

Rigidity0increased resistance to passive movement cogwheel quality

Bradykinesia-slowness of movement ; often difficulty initiating movement

168
Q

Progressive supranuclear palsy

A

Bradykinesia and rigidity

Loss of voluntary control of eye movements (vertical gaze)

169
Q

MSA Shy Drager syndrome

A

Bradykinesia and rigidity

Pronounced an autonomic dysfunction

170
Q

Cortical basal degeneration

A

Both cortical and basal ganglionic dysfunction
Bradykinesia and rigidity
May also see cortical sensory loss, apraxia, myoclonus or aphasia

171
Q

Anti parkinsonian medications have little effect on other akinetic rigid syndromes

A

PSP, MSA, CBD

172
Q

Anti parkinsonian treatment

A 
Dopamine agonists (bromocriptine)
Levodopa
COMT inhibitors 
Anticholinergics
MAO-B inhibitors
Amantadine
Surgery
173
Q

Hyperkinetic movement disorders

A

Chores , athetosis, dystonia, ballistics, Tic

174
Q

Sydenham’s chorea

A

In kids as complication of a previous infection with group A hemolytic step . May be arteritis

Characterized by unilateral choreiform movements which when mild can be confused for restless or fidgeting. May also see behavioral changes

175
Q

Treat Sydenham’s chorea

A

Bed rest and antibiotics

176
Q

Idiopathic torsion dystonia

A

Characterized by dystonia movements and postures without other signs
May be inherited AD, AR, or X linked

Onset may be childhood or later life, but remains throughout life

177
Q

Idiopathic torsion dystonia

A

Torticollis, blepharospasm, oromandibular dystonia, arm may be held in hyperpronated position with wrist flexed and fingers extended
Leg may be held in extension, with pronation and inversion of the foot

178
Q

Treat idiopathic torsion dystonia

A 
Low doses levodopa
Anticholinergics
Benzodiazepines
Neuroleptic drugs
Baclofen
Carbamazepine
179
Q

Focal torsion dystonia

A

Dystonia confined to focal area
Blepharospasm
Oromandibular dystonia
Spasmodic torticollis

Writers cramp

180
Q

Treat focal torsion dystonia

181
Q

Wilson’s disease

A 
AR copper metabolism dysfunction that produces neurologic and hepatic dysfunction 
Chromosome 13(gene ATP7B involved in transportation of copper)
Decreased binding of copper to ceruloplasmin leading to large amounts of free copper deposited into tissues

Presents in childhood or young adult life

182
Q

Clinical features Wilson’s disease

A

Bradykinetic and hyperkinetic features

Resting or postural tremor
Choreiform movements

Rigidity
Bradykinesia
Dysarthria, dysphagia
Ataxia
Personality/behavioral changes
Dementia
Psychosis/hallucinations
183
Q

Diagnosis Wilson’s

A

Based on history, exam findings
Increased amounts of copper excretion in 24 hours urine collection
Decreased serum ceruloplasmin level
Kayser fleischer ring on eye exam

184
Q

Treat Wilson

A

Penicillmaine (a copper chelating agent

Restriction of dietary copper

185
Q

Tic disorders

A

Single motor tics (blinking, coughing, throat clearing)) often occur as a benign entity

Gilles de la Tourette’s syndrome-chronic multiple motor and vocal tics with onset before the age of 21

186
Q

Gilles de la Tourette’s syndrome

A

Most cases sporadic
Males
Vocal tics vary in presentation, but can involve barks, hisses, grunts, throat clearing, coughing among others

See-coprolalia (vulgar or obscene speech), echolalia (parroting speech of others), echoproxia (imitation of others movements), palillalia (repetition of words of phrases)

187
Q

Treat Gilles de la tourettes

A

Clonidine
Haloperidol
Phenothiazines

188
Q

Essential tremor (benign familial tremor) clinical presentation

A

Postural or kinetic tremor of both hands and may involve the head or voice

Can begin in early adulthood but often not until later in life

Usually progresses slowly over year to decades

Usually does not results in significant disability, but social embarrassment is common
EtOH often decreases the tremor temporarily

189
Q

Treat essential tremor

A

Beta blockers
Primidone
Benzodiazepines
Topiramate

Deep brain stimulation

190
Q

Dementia

A

Decline in memory and at least one other cognitive function (aphasia, apraxia, agnosia, exucitve function)
-decline impairs social or occupational functioning in comparison with previous functioning. These deficits should not occur exclusively during the course of delirium and should not be accounted for by another psychiatric condition such as depression or schizophrenia

191
Q

Incidence and prevalence of dementia

A

10% over 65

More than 30% over 85

192
Q

Causes of dementia

A 
Degeneration 
Vascular
Infectious
Psychiatric (including alcohol)
Toxic/metabolits(B12, thyroid)
Traumatic
Tumors(astrocytoma/glioblastoms, lymphoma, metastatic tumor)
Other(hydrocephalus)
193
Q

Evaluation of patient with dementia

A

History, patient difficulting (safety, function, memory, time course, family history dementia)

Mental status test
Look for CVD risk factors
Full neurologic exam

Lab-CBC, chemistrypanel, Syed rate, thyroid function studies, RPR, CT or MRI of the head, EEG, LP, HIV, CXR, drug screen, SPECT, PET< heavy metal

194
Q

Diagnosis of AD

A

Dementia (mini mental state exam)
Deficits in 2 or more ares of cognition
Progressive worsening of memory and other cognitive function
No disturbance of consiousness
Onset between te ages of 40 and 90 yr, most often after65
Absence of a systemic disorder or other brain diseases that in and of themselves could account for the progressive deficits in memory and cognition

195
Q

Supporting finding in the diagnosis of probably AD

A

Progressive deterioration of specific cognitive function such as aphasia, apraxia, or agnosia
Impaired activities of daily living and altered patterns of behavior
Family history of similar disorders, particularly if confirmed neuropathologically
Normal LP
EEG: normal or mild generalized slowing
Progressive atrophy documented by MRI or CT brain

196
Q

Treat AD

A 
Slow progression 
Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)

NMDA receptor antagonist (Memantine)B complex, lipid lowering agent, asprin

197
Q

Mild cognitive impairment

A

Memory complaint, often noted by the patient

Tested abnormal memory for age, and yet does not meet the criteria for dementia(normal cognitive function and daily living)
Probably a precursor to AD
Patients with MCI are 5x more likely to develop clinically probably AD than age matched control s
Treatment with AchEI medications may slow progression to AD

198
Q

Criteria for vascular dementia

A
  1. Cerebrovascular disease defined by the presence of focal signs neurologic examination, such as hemiparesis, lower facial weakness, babinski sign, sensory deficit, hemianopia, consistent with stroke
  2. Evidence of relevant cerebrovascular disease at brain imaging including multiple large vessel infarcts or a single strategically situated infarct(angular gyrus, thalamus, basal forebrain, or posterior or anterior cerebral artery territories), as well as multiple basal gangliaand white matter lesions and white matter lacunas or extensive periventricular white matter lesions or combination threof
  3. A relation between cognitive problems and vascular events manifested or inferred by the presence of one or more of the following
    - onset of dementia within 3 months after a recognized stroke
    - abrupt deterioration in cognitive function OR
    - fluctuating, stepwise progression of cognitive deficits
199
Q

Diffuse Lewy body disease

A

Dementia, parkinsonian, prominent psychotic symptoms, EXTREME SENSITIVITY TO ANTIPSYCHOTIC AGENTS

200
Q

Diffuse Lewy body disease

A
  • often progresses more rapidly than AD
  • symptoms generally vary a great deal more from one day to the next than do symptoms in AD
  • up to 81% of patients with diffuse ley body have unexplained periods of markedly increased confusion that last days to weeks and closely mimic delirium
  • mild to moderate parkinsonian features are often present early int he disease. Bradykinesia, rigidity and falls are often prominent. Tremor is usually absent. Response to L dopa is poor
  • dysautonomia is common
  • psychotic symptoms are mush more common and occur earlier in diffuse Lewy body disease that AD
  • visual hallucinations is the most common psychotic symptom-generally animals or people, often children
  • these hallucinations are often not particularly bothersome
201
Q

Beware. Most patients with diffuse Lewy body disease experience severe, potentially life-threatening adverse reactions if treated with ___ ___

A

Antipsychotic agents

If an antipsychotic is truly needed, use one of the newer agents (quetiapine or olanzapine)

202
Q

Parkinson

A

Midbrain Lewy bodies
Executive dementia sometimes occurs late in illness
Resting tremor usually resent
Autonomic dysfunction sometimes seen
Hallucinations only in response to anti parkinsonian drugs

203
Q

Diffuse Lewy body disease

A

Cortical Lewy bodies
Cortical dementia always occurs early in illness
Resting tremor usually absent
Autonomic dysfunction prominent
Hallucinations common in absence of anti parkinsonian drugs

204
Q

Frontotemporal degeneration

A

Progressive deterioration of social skills and changes in personality, along with impairment of intellect, memory and language

Varies greatly int he way it affects individuals, but often see common core symptoms(loss of memory, lack of spontaneity, difficulty in thinking or concentrating, disturbances of speech)

Other symptoms include:gradular emotional dullness, loss of moral judgement, and progressive dementia

Usually affects individuals between ages 40 and 60

Patients typically have atrophy of the frontal and temporal lobes of the brain

No cure. Length progression 2-10 years

205
Q

Triad of hydrocephalus

A

Dementia
Gait
Urinary incontinence

206
Q

Hydrocephalus is potentially reversible with ____ ___

A

Ventriculoperitoneal shunting

207
Q

What symptom is most likely to be reversed in normal pressure hydrocephalus with ventriculoperitoneal shunting

208
Q

CADASIL

A

Cerebral autosomal dominant ubcortical infarcts and leukoencephalopathy

209
Q

Onset CADASIL

210
Q

Inheritance CADASIL

A

NOTCH3 gene on chromosome 18 causing progressice degeneration of smooth muscle cells in BV

211
Q

Manifestation of CADASIL

A

Migraine HA and TIA or strokes. MRI shows abnormalities of multiple areas of ischemia years prior to the onset of symptoms

212
Q

Progression of CADASIL

A

Subcortical dementia

213
Q

Treating CADASEIL

A

Genetic test and sometimes skin biopsy to look for typical arteriopathy

214
Q

Treat CADASIL

A

Antiplatelet agents, and efforts to minimize risk factors for vascular disease are helpful

No specific treatment

215
Q

Stroke

A

5th leading cause of death in US, leading to long term disability, 133000 die annually, survivors have residual impairment , pregnancy and post partum

216
Q

Subtypes of. Stroke

A

Hemorrhagic and ischemis

217
Q

Hemorrhagic stroke 20%

A 
Intracerebral hemorrhage (cortical vs subcortical)
Subarachnoid hemorrhage
218
Q

Ischemic stroke 80%

A 
Large artery atherosclerosis with thromboembolism 
Small vessel (lacunar ) disease
Cardioembolism 
Nonatherosclerotic vasculopathies
Hypercoagulable states
219
Q

Risk factors for stroke

A 
Age
Previous TIA or stroke 
Atherosclerosis
CVD
Drug abuse
Oral contraceptive
Pregnancy post partum 
Fibromuscular dysplasia
Hypercoagulable states
Inflammatory disorders
220
Q

Symptom of stroke in left hemisphere

A

Aphasia, right sizes sensory symptoms, right sided motor symptoms, right visual field cut

221
Q

Symptoms of right hemisphere stroke

A

Left hemineglect, left sided sensory symptoms, left sided motor symptoms, left visual field cut,

222
Q

Symptoms of cerebellar stroke

A

Ipsilateral ataxia, vertigo, nystagmus

223
Q

Symptoms of brainstem stroke

A

Cranial nerve findings with contralateral hemisensory or hemimotos symptoms, vertigo

224
Q

Generate management of stroke

A

Primary prevention, management of the acute stroke
Prevention or control of medical complications (complications account for 50% of death)
Rehab
Prevention of recurrent stroke

225
Q

Emergent diagnosis and treatment of stroke

A 
ABS, BP, pulse, cardiac monitor, EKG, O2 saturation 
IV access
Neurological examination 
Labs
NIH stroke scale
226
Q

Acute HTN is common in acute ischemic stroke and in msot cases should __ be treated

227
Q

The area of infarction may have lost autoregularoy function, so that normal BP may be relatively ___ in the brain

A

Hypotension

228
Q

All stroke patients need IV access

A

Should not include glucose as hyperglycemia is associated with worse neurologic outcomes
If tPA is a consideration two IV access sites will be needed to eliminate venipuncture after infusion

229
Q

Labs for stroke

A

CBC, PT, PTT, full chemistry panel and fingerstick glucose, UA, CXR

230
Q

The NIH scale is important if tPA or intra-arterial intervention is a consideration. Describe scores

A

Score ranges from )(normal) to 43 (coma) and can be used to predict hemorrhagic conversion as well as indication for potential intra-arterial intervention

Score<10=2-3% risk of hemorrhage
Score>20-17% risk of hemorrhage

231
Q

Summary of Eval and tax of acute stroke

A 
Maintain ABS
Elevate HOB 30 degrees
O3 3 liters per NC
Vitals, establish IV with NX
CBC, PT, PTT, Chem
EKG
Obtain patient weight
Try to identify cause and treat fever if present 
Get history CT
232
Q

What history is important for stroke

A 
Last time without symptoms 
Trauma cause onset
Warfarin/heparin or NOAC?
Symptoms of MI
Symptoms of intracranial hemorrhage
233
Q

CT findings stroke

A

Cerebral infarction (if patient meets all tPA criteria, consider administering tPA if absolutely sure of time deficits began

Normal -consider another cause:seizure, migraine, hypoglycemia
-if history most consistent with ischemia, consider tPA or other therapies (ASA, aggrenox, ticlid, plavix)

234
Q

IV tPA with stroke eligibility criteria

A

Over 18
Diagnosis of ischemic stroke with clinically apparent neurological deficits
No stroke or head trauma in preceding 3 months
No major surgery in preceding 14 days
No h/o intracranial hemorrhage
No rapidly resolving symptoms or only minor symptoms of stroke
No symptoms suggestive of SAH
No GI or GU hemorrhage preceding 21 days
No symptoms suggestive SAH
No arterial puncture at non compressible site in preceding 7 days
No seizure at onset of symptoms
PT<15 sec or INR<1.7 without warfarin
PTT within normal range if heparin awas given in preceding 48 hours
Platele ycount >1000000
Blood glucose>50 mg/dl
SBP<185 and CBP<110 mmhg and no need for aggressive measures to lower BP

235
Q

How treat acute ischemic stroke with IV tPA

A
  • infuse tPA at a dose of .9mg/kg (max 90mg) over a 60 min. Period with the first 10% of the dose given as a bonus over a 1 min period
  • perform neuro assessments and check BP q 15 min. During infusion every 30 min. For 6. Hours after and then every 60 min for the next 12 hours
  • if severe HA, acute HTN, or NV occur, stop infusion and obtain an emergent CT head
  • If SBP>180 or DBP>105 mmHg, check BP more frequently and give anti-HTN drugs as needed to maintain BP at below those levels
236
Q

Anticoagulation and stroke

A

Acute anticoagulation with heparin was sometimes used in past to
-prevent of limit progression in patients with acute atherothrombotic infarction, or prevent recurrent embolism in patients with cardio embolic stroke

Early studies suggest 50% reduction int he chance of neurologic worsening, particularly for subcategories of TIA and stroke in progression
-but bad….little role of anticoagulation ins trope patients

237
Q

Other agents to treat stroke

A 
Asprin
Aggrenox
Ticlopidine 
Clopidogrel
Dipryidamole
Warfarin
Low molecule weight heparin 
Dagibatran etexilate
Riveroxaban
Apixaban
238
Q

What are the clinical situations in which warfarin (NOACs are newer) indicated for

A 
Atrial fibrillation 
Prosthetic valve
MI
Atrial septal defect
Hypocoagulable state
Large vessel disease
Aortic arch disease
239
Q

Combination therapy for stroke

A

ASA and plavix-espicially in the first few weeks after stroke (avoid long term due to increased risk of GI bleeding)

240
Q

In addition to emergent CT scanning of hte brain, what other studies may be done for stroke

A

CT perfusion studies, MRI, MRA, diffusion weighted and perfusion weighted MRI, transcranial soppler ultrasonography, CT angiography, xenon enhanced CT, single photon emission CT and cerebral angiography

The above test would be selected to establish the anatomical regions and structures involved and the cause of the infarct , thereby choosing appropriate intervention

241
Q

Carotid angioplasty with stent placement

A

Early data says lower risk of complications than CEA

Consider when patient at high risk for surgery-CAG or valvular heart disease carotid disease or bilateral severe carotid disease

242
Q

Endovasculr therapy(intra-arterial thrombolysis with clot retrieval

A

MOST PROMISING

SIGNIFICANT IMPROVEMENT IN PATIENT OUTCOME COMPARED TO STANDARD THERAPY

MULTIPLE STUDIES WHOWING IMPROVEMENT IN PATIENTS TREATED WITH ENDOVASCULAR/INTRA-ATERAIAL INTERVENTION IN ADDITION TO TPA WHEN COMPARED TO TPA USE ALONE

243
Q

ACUTE ISCHEMIC STROKE IS AN _____

244
Q

How can we get patients to ER sooner

A

Learn symptoms and signs for early ischemis

245
Q

First thing ask when see patient

A

Can it be localized?

246
Q

Speech disturbance

A

Left cortical hemisphere localized

247
Q

Patient sleepy and weak all over

A

Not localized

248
Q

Number one thing after history and exam

A

Can i localize it

249
Q

Second thing

A

Broad categories of what might be causing presentation

250
Q

80 yr old patient with a fib dimished heart function cant speak or move right side

251
Q

Broad categories

A

Congenital/genetic, vascular, tumor/paraneoplastic, infection, inflammation/autoimmune.toxic/metabolic/degenerative/episodic/psychiatric

252
Q

3rd thing

A

Design testing and treatment plan keeping in mind differential diagnosis

253
Q

Can things be in both categories

A

Yea vascular genetic

254
Q

Episodic disorder

A

Migraines?

255
Q

Todd’s paralysis

A

Can’t speak weakness on right side

256
Q

Primary migraines

A

Cluster

Tension

257
Q

Classic

258
Q

Common

A

Without aura

259
Q

Aura

A

Anything neurological but most commonly visual usually 15-30 minutes

260
Q

Migraine F or M

261
Q

Age onset migraine

262
Q

Severity headache

A

Moderate to severe

263
Q

Quality headache migraine

A

Throbbing, sharp, severe pressure,

264
Q

Associated symptoms migraine

A

Nausea, photophobia, sensitivity to light, phonophobia/sonophobia,

265
Q

How long are migraines

A

Hours to days

266
Q

Trigger migraine

A

Unknown, stress/letdown , food (MSG), sharp cheese, red wine , chocolate, any food, bright lights, sleep deprivation, change in sleep cycle, hormones (estrogen, BCP, hysterectomy, onset menses, ovulation, exogenous hormone (not progesterone), weather change(storms), smells,

267
Q

chronic migraine

A

Chronic migraine 15 or more head ache days over 4 hours for at least 3 months -don’t have to be severe, often dull achey

268
Q

Drug of choice for chronic migraine

A

Only FDA approved is Botox injections done every 90 days

269
Q

Cluster headache

A

Vascular, men, unilateral, periorbiatal, sharp boring, penetrating, once pick, severe, excruciating, pacing and rocking, can’t sit still, last 45 minutes (5 hours is not cluster), can occur more than once in day, often seasonal FALL

270
Q

Prevent cluster headache long term treatment -when get 2 or three times a year or its not predictable then they get

A

Verapamil is more common oral (ca channel blocker)**, fewer side effect
Valproic acid-but not young women, get fat on it too
Lithium

271
Q

Prednisone/steroids cluster head ache REACTIVE get it in December for example-start when get cluster headache

A

Treat

Cluster head ache give if get once one for a few weeks

272
Q

Who do we not give valproic

A

Young women unless absolutely no other option

273
Q

Other cluster symptoms

A

Burning nostril and inner canthus of eye on side, flushing of face on that side

Sleep apnea

274
Q

Secondary headache

A 
Worrisome or sign of organic disease
Worst head ache of life
Over 50 
Abrupt 
Abnormal exam 
Loss of sensation 
Weakness on one side
Babinksi
Visual field cut
Toe up 
Fever
DO WORKUP IF HAVE THIS
275
Q

Presentation for ruptured cerebral hemorrhage

A

Thunderclap headache, severe abrupt onset headache , grab head scream OMG my head and fell down,

276
Q

PCOM posterior cerebral artery symptoms -uncal herniation

A

CN3 palsy eye down and out
Pupil dilated no parasympathetic (parasympathetic fibers run along outside of third nerve so aneurysm push on it , hit parasympathetic fist)

1st see blown dilated pupil as prescribed harder then get down and out hit axons of third nerve /and stuperous

3 hours later-patient not responsive cant arouse and funny movements DECEREBRATE POSTURING ON CONTRALATERAL SIDE

Bad sign get on phone with neurosurgeon

277
Q

What test when see the pupil in and out and stupor

A

Put in CT now! Look for subarachnoid hemorrhage

Bright white see it surrounding meninges

278
Q

What do when see subarachnoid hemorrhage on CT

A

Sedate, ventilation, call neurosurgeon, DO NOT NEED LP not safe

279
Q

What if CT is negative for subarachnoid hemorrhage

A

LP could be 5-10% of subarachnoid hemorrhage on CT and need LP to look for it and rule out other stuff

280
Q

Trigeminal neuralgia

A

Pain sharp electrical pain in little paraoxysms last seconds maybe a minute or two
Off and on all day long
Little in and out

281
Q

What triggers trigeminal neuralgia

A

Chewing talking hot liquids cold liquids frozen food super hot foods brush teeth

282
Q

Drug for trigeminal neuralgia

A

Carbamazepine

Oxcarbazepine-better

283
Q

Wilson’s disease

A

Liver and brain
Copper
Young ppl

284
Q

Don’t catch Wilson

285
Q

Wilson treat

A

Reverse or cure

286
Q

Bradykinetic or hyperkinetic wilson

287
Q

Balism

A

Large flinging

288
Q

Brief dance like fidget/tic

289
Q

Sustained position extension arm extension finger(can get lot of places

290
Q

Myoclonus brief jerking movements

291
Q

Friedreich ataxia

A
  1. Ataxia (falls, balance disturbance, dimished strength, areflexia)
  2. Young ppl
  3. Die from cardiomyopathy
292
Q

Akinetic rigid syndromes

293
Q

Most common parkin

A

Idiopathic PD

294
Q

Features parkinson

A

Tremor resting or pill rolling UNILATERAL(idiopathic), rigidity, Brady, soft voice, stare, dimished eye blink, myerson sign(tap on forehead),

295
Q

Drug induced parkinson

296
Q

MSA

A

Autonomic dysfunction pronounced with stiffness and slow

297
Q

CBD

A

Cortical

Hemiparesis, apraxia, stiff slow

298
Q

PSP

A

Eyes vertical gaze
Volitional
If more head eyes do what supposed
If ask them to move up and down they cant

299
Q

Lewy body disease

A

Slow stiff
Dementia
Hallucinations (visual-little mice, imposter syndrome)-can get in parkinson but only in drug induced parkinson

Early psychotic visual hallucinations
Akinetic and rigid family say they fall all the time often backwards
-delirium are way off encephalopathic
80% crazy then back to self

-don’t treat automatically bc very sensitive to antipsychotic meds and can be life threatening

300
Q

AD

A

Memory loss
Progresses
At least 2 domains (memory loss and speech disturbance) can become psychotic as well(late-kids try to steal money or spouse having affair, or someone stole stuff when misplaced often directed at people they’re closest to) in Lewy body psychotic is early

301
Q

MS

A

Central nervous system (spine brain) not peripheral

302
Q

Most common MS

A

Relapsing remitting MS -exacerbations and remissions , have spell and get better then have another attack

Test cant diagnose 1
Look for MRI, LP, oligoclonal bands igG synthesis rate index igG immunoglobulin and sample of blood ratio igG and CSF to blood in case of MS see abnormalities have more igG in spinal fluid than blood .
Index up synthesis up

303
Q

Recognize disease modifying MS meds on routine maintence basis

A

Leterium acetate, monoclonal antibodies (MABS-MAB at end)
Interferons, dimethylfumurate, fingolamide

These are not for symptomatic treatment they are disease modifying to change course of disease

304
Q

Drugs for acute attack of MS/shorten course of exacerbation but don’t change overall course of disease

A

Corticosteroids
IV prenisolone
ACTH acthar gel
STEROIDS

305
Q

Spasticity med

A

Baclophan

Trendazoline

306
Q

Neuropathic pain

A

Pregabalin

307
Q

Stimulants

A

Methylfenodarte for severe fatigue

308
Q

Mimickers of MS

A

Clinically isolated syndrome

  • monofolcal (1 lesion correlated with 1 symptom
  • multifocal, acute disseminated myeloencephalitis can be confused and become MS(multiple lesions at 1 time, wait to see if have MS or one and done —-MS is multiple over space and time)
309
Q

Epilepsy

A

Partial or focal can secondarily generalize-begin on one side
(Kindling could spread to major motor generalized seizure)
Primary general-
Idiopathic genetic, both sides

310
Q

Generalhow many need to have epilepsy

A

2 or more unprovoked—alcohol withdrawal doesn’t count, what if one happened with tramadol or something NO not unprovoked
In certain cases can make diagnoses with one seizure and abnormal EG

311
Q

Most important to epilepsy diagnosis

A

History form witness———what did they look like

312
Q

EEG normal and think have epilepsy

A

Can miss it may have epilepsy

313
Q

What if see episode on EEG but don’t think epilepsy

A

Don’t have

314
Q

99% seizure on EEG

A

Absence seizure wha3 hz spike per second

Starts on both sides of brain initially

Primary generalized or idiopathic

315
Q

Absence

A

Ethosuximite

316
Q

If major motor seizure and absence

A

Ethosuximite and broad spectrum whether partial or generalized

  1. Valproic acid (not young woman)
  2. lamotrogine-works and lowest side effects and safe in pregnancy 2/3 patients first drug will work
  3. Levotoracitam
  4. Zonisamide
317
Q

Zonisamide and topiramate

A

Kidney stones-so if history move to something else

318
Q

Try to use one drug or more

319
Q

New are better and new effective

A

Start with newer drugs

320
Q

Most common reason for breakthrough seizure in well controlled for years

A

Noncompliance missed meds

321
Q

Absence

A

Abrupt stop and abrupt start on ecg

322
Q

What can accompany major motor seizure

A

Lateral part of tongue bite
Urination , bowel incontance
Post ictal state-lethargic tired confused

323
Q

Transient global amnesia

A 
1 and done does not recur 
Amnesia only ! Lasts hours 3-6
Patient asks the same questions over and over again scares people 
By time consult comes its resolved 
Very common
324
Q

Stroke

A

Sudden like lightening

325
Q

2 types stroke

A

Ischemic-80%

Hemorrhagic 20%

326
Q

Risk for stroke

A

Hypertension, tobacco, age, DM, TIA or previous stroke, cardiac arrhythmia, A fib high risk, mural thrombas from old MI, left ventricle from heart attack, idiopathic, cardiomyopathy, not pumping does sound familiar, ejection fraction measure how much blood pumped out 2-% or less bad ventricular function high risk of getting clot on left ventricle that shoot out that’s the 20%

327
Q

Med to prevent stroke

A

Asprin

Clavix,

328
Q

Multiple stroke treat A fib, ejection fraction less than 20% (cardiomyopathy) prevention of stroke , prosthetic valve
To prevent still not at treatment

A

Warfarin or NOAC(newer oral anti coagulation)

329
Q

Acute stroke

A

Don’t want glucose blood sugar?
Passive hypertension to increase perfusion
(Don’t want to lower it) allow for a while (let it be high for 2 weeks then manage it)
Fever
ABC always check

330
Q

Treat acute stroke

331
Q

What can cause focal neurologic prob and be confused with stroke ABRUPT

A

Primary headache disorder migraine with aura (tingling, work finding difficulty)

Metabolic abnormalities
Hyperglycemia
Hepatic

332
Q

Coma

A

Both cerebral hemispheres effected or brainstem effected

333
Q

Lesion in pons

334
Q

Lesion in medulla

335
Q

Small thalamus, hypothalamus, one side

A

No need both hemispheres

336
Q

What is periventricular white matter abnormalities on both side

A

No haven’t effected cortex so no coma

337
Q

Coma from herniation hallmark

A

Anesecoria, pupillary abnormality -don’t see if have hepatic dysfunction or glucose stuff

338
Q

Hepatic encephalopathy examination-can get neurologic

A

Asterixis

Extend arms extend wrist see twitchy movements

339
Q

Progression of loss of function in brain of anoxic patients reverse teleological area. Oldest teleological most resistant to anoxia

A

First lose most well developed(last to develope are first to go)-cortex

  1. Lose corneal reflex and pupillary responses level of midbrain
  2. Oculocephalic-mid pone (water in ear)
340
Q

Mild anoxia

A

Memory loss confusion

341
Q

Brain death

A

Specific definition know it

342
Q

Patient has 103 fever stiff neck encephalopathic or comatose

A

ABC
O2 state, EKG, glucose, CBC, CMP , quick history

Cat scan negative then do LP

343
Q

If diffuse edema and herniation on cat scan

A

Do not do LP brain stem herniation into spinal canal

344
Q

AD vs Lewy body

A

Hallucinations early lewy-usually visual

Hallucination late in AD-usually paranoia

345
Q

1st AD

A

Short term memory language word finding can get paranoid or aggressive later on

346
Q

MRI Ad

A

Generalized atrophy

347
Q

Normal pressure hydrocephalus triad

A

Gait-falling
Urinary incontinence
Dementia (cognitive impairment )

348
Q

NPH

A

Progressive onset in less than a year

349
Q

MRI NPH

A

Enlarged ventricles without obvious obstruction

350
Q

Treat NPH

A

Shunt neurosurgeon shunt decrease space of ventricles sometimes help sometimes not

Gait improves first

351
Q

Vascular dementia —hemiparesis upgoing to, sensory loss incordination in one hand, visual field cut-something says focal

A

Step wise progression-fine fine fine then terrible stable stable stable, another abrupt —multiple over time take patient down

Or

Massive single strategically placed stroke-left hemisphere cant communicate and demented unless improve
ONE event

352
Q

Nystagmus of labrinthial

A

Horizontal nystagmus

Don’t see vertical or pendular nystagmus

353
Q

Ménière’s disease

A

Hearing los
Low frequency
Tinnitus -crickets high frequency , high pitched funny noise cant go to sleep, dull fullness sensation in ear. Funny fullness sensation

Most of people lose high frequency

354
Q

Teat menieres

A

Low sodium diet
Diuretics

Low dose Valium will also fix

355
Q

Toxins that can cause vestibular dysfunction

A

Alcohol and
Chronic-cerebellar dysfunction can cause

Antibiotics-aminoglycocides gentomycin

356
Q

Rhomberg test

A

Feet together arms to side close eyes
If able to stand with eyes open ok then close and cant keep balance

Have proprioceptive abnormality rhomberg positive

Testing proprioceptive pathways

357
Q

Benign paroxysmal vertigo initially presentation BPPB

A

Patient awakens and feel fine don’t

Severe vertigo vomiting nausea, cant keep balance ,

358
Q

What do to test BPPV POSITIONAL one position fine other and not fine

A

Dicks hall pike maneuver turn one way ok turn other way and get symptoms tells us labyrinth and BPPV

Vestibular neuritis is also labyrinth and no different in turning other way

359
Q

Orthostatic hypotension

A

Laying to standing systolic change 20 diastolic Change of 10

Describe light headed dizzy faint when upright head
Dizzy upon standing relieve symptoms when lay down
Also worse in morning -been flat long time

360
Q

MS drugs disease modifying change overal outcome

A

Interferons, monoclonal antibodies, literium acetate, dimethylfumerate

361
Q

Steroids

A

Not disease modifying

362
Q

Symptom treatment spasticity

A

Baclofen ????

363
Q

Gabapentin pregambalin

A

Neuropathic pain

364
Q

3d diffusion tensor imaging

A

Look for axonal injury in periventricularwhite matter

365
Q

Student athlete concussion and headache nausea

A

Do not let them do sport

366
Q

Student athlete no symptoms

A

May let them do light aerobic exercise

367
Q

Mild symptoms

368
Q

When see again

A

A few days later

369
Q

Symptoms after aerobic exercise

370
Q

Treatment for consussion

371
Q

Dopamine vs serotonin effective

A

Dopamine-cognition OK, compulsive(reward system), irritable,

Serotonin SSRI-inhibit reuptake, treat mood disorders-have mood disorders, depression, irritability, anxiety, decreased COGNITION, sleep disturbance,

Pharmacology (52 decks)

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